We have found that animals fed a diet containing cyclocreatine, an analog of creatine, accumulate high concentrations of cyclocreatine-P (1-carboxymethyl-2-imino-3-phosphonoimidazolidine), an analog of creatine-P, in heart, muscle, and brain. Prolonged feeding of cyclocreatine results in delay of onset of rigor in ischemic heart and skeletal muscle. In skeletal muscle glycogenolysis and turnover of high energy phosphate are decreased by feeding of cyclocreatine. In contrast to the case of skeletal muscle, we have found that the glycogen content of heart is markedly increased during cyclocreatine feeding. This might account for the delayed onset of rigor during ischemia. We plan to investigate this phenomenon more closely and study the effects of certain hormones known to affect heart metabolism on hearts of rats fed cyclocreatine and several novel analogs of cyclocreatine, including ethylcreatine and homocyclocreatine. We have found that these latter two analogs are also accumulated as their high energy phosphate derivatives in heart and the physiological effects of these accumulations will be explored.